Bulimic syndromes (BN-S) are characterized by large out-of-control binge episodes, span the three DSM-5 eating disorder categories of anorexia nervosa-binge purge subtype (ANbp), bulimia nervosa (BN), and binge eating disorder (BED), and vary considerably in illness severity and course. Our long-term objectives are to identify biobehavioral predictors of illness trajectory in BN-S so that treatments may be developed to address key factors influencing the severity and course of binge eating. The specific aims of this study are to test a model in which weight suppression (WS) leads to deficient circulating leptin, which contributes to blunted postprandial glucagon-like peptide 1 (GLP-1) response, which causes alterations in the RDoC core constructs of approach motivation and sustained responsiveness to reward, which then contribute to BN-S severity and maintenance. WS (the difference between an individual's highest weight and current weight) has emerged as one key predictor of severity and maintenance of BN-S, and investigators have posited a biobehavioral mechanism for this association. Yet, no study has evaluated how the biological consequences of WS may contribute to alterations in RDoC core constructs proposed to contribute to binge eating. Our model posits that the same set of physiological consequences of WS contribute to binge eating by 1) increasing drive/motivation to consume food (approach motivation), and 2) decreasing ability for food consumption to lead to a state of satiation/satisfaction (sustained responsiveness to reward). Approach motivation will be measured both behaviorally as breakpoint on progressive ratio tasks for food and non-food reinforcers and by self-report. Sustained responsiveness to reward (satiation) will be measured both behaviorally as food intake in an ad lib meal and by self-report. Participants (N=320) with BN-S and non-eating disorder controls, ranging in BMI from 16 to 35 kg/m2, will be assessed for WS, leptin, GLP-1 response to a fixed meal, approach motivation, ability to achieve satiation in an ad lib meal, self-report measures of core constructs, and binge eating at baseline, 6-, and 12-month follow-up, to produce the first study of biobehavioral predictors of illness trajectory in BN-S transdiagnostically. Examining the integration of approach motivation and satiation through the same set of physiological mechanisms represents a major innovation as it translates cutting-edge research in basic science to understand clinical phenomena in BN-S. If differences in illness trajectory across ANbp, BN, and BED are attributable to the underlying dimension of WS, this will fundamentally alter conceptualization of BN-S from three eating disorder categories to one eating disorder. If findings support biobehavioral distinctions across the BMI range, this would provide important information in what treatments would work in whom. Moreover, our focus on factors that are modifiable via behavioral and pharmacological interventions increases the public health significance of this work by facilitating novel treatment approaches to ameliorate distress, disability, and death in syndromes accounting for an important segment of those suffering from eating disorders.